Hyponatremia — low sodium in the blood — is the most common electrolyte disorder you'll see in the clinical setting, and one of the most confusing, because several different mechanisms can drive it.
Sodium is central to fluid balance, nerve transmission, and muscle contraction, so any imbalance can cause major problems. This guide breaks hyponatremia down so you can identify it, understand the cause, and manage it safely at the bedside.
Before getting into hyponatremia itself, three fundamentals make the whole topic click: diffusion, osmosis, and osmolality.
Diffusion
Molecules move from higher to lower concentration until equilibrium. In the body this moves nutrients and waste across cell membranes.
Osmosis
Water moves across a semi-permeable membrane toward higher solute concentration. When blood sodium is low, water shifts into cells and they swell.
Osmolality
A measure of total solutes in a solution. Sodium is a major contributor, so when osmolality is off, cell hydration and function suffer.
Why it matters: in hyponatremia, low blood sodium lowers serum osmolality, so water moves into cells — including brain cells. That cellular swelling is what drives the dangerous symptoms.
Why Is Sodium Important in the Body?
Sodium runs several physiologic processes at once, which is why a low level can disrupt so many systems.
Fluid Balance
Sodium attracts and holds water in the right compartments — where sodium goes, water follows.
Blood Pressure
By influencing blood volume and vessel wall tension, sodium helps regulate blood pressure.
Nerve Transmission
Sodium generates and propagates action potentials — the electrical signals neurons use to communicate.
Muscle Contraction
With potassium and calcium, sodium initiates the signals that make muscles contract and relax.
pH Balance
Sodium participates in the mechanisms that keep the body's acid-base balance in a narrow range.
Nutrient Absorption
Sodium aids absorption of nutrients in the small intestine — glucose uptake is often sodium-coupled.
How Is Sodium Regulated in the Body?
Sodium is controlled by several organs and hormones working together, mostly at the level of the kidney.
The Kidneys
Filter blood and selectively reabsorb sodium, retaining or excreting it as needed — largely directed by aldosterone and ADH.
Aldosterone
From the adrenal glands. Tells the kidneys to keep more sodium (and water with it), raising blood volume and pressure.
Antidiuretic Hormone (ADH)
Vasopressin, from the pituitary. Makes the kidneys reabsorb water, diluting the blood — indirectly affecting sodium concentration.
Atrial Natriuretic Peptide (ANP)
Released by the heart when the atria stretch. Promotes sodium excretion to lower blood volume — a counterbalance to aldosterone.
Dietary Intake & Thirst
Food and drink supply sodium; thirst drives water intake when sodium is high. Thirst is less reliable in elderly patients.
Normal Sodium Levels & Hyponatremia
Normal serum sodium runs 135–145 mEq/L. Anything under 135 is hyponatremia, graded by severity:
Normal
135–145
mEq/L
Mild
130–135
mEq/L
Moderate
120–130
mEq/L
Severe
< 120
mEq/L
Acute vs Chronic Hyponatremia
Before treating, you need to know whether the drop was acute or chronic — it changes how aggressively sodium can be corrected.
Acute (< 48 hours)
Sodium drops too fast for brain cells to adapt, so they swell. Can cause headache, vomiting, seizures, respiratory arrest, and herniation. Treated more aggressively.
Chronic (> 48 hours)
Slow onset lets cells adapt, so symptoms are milder (nausea, headache, confusion, fatigue) or absent. Must be corrected cautiously.
Causes of Hyponatremia
Hyponatremia is fundamentally an imbalance in the body's sodium-to-water ratio. Evaluating serum osmolality alongside sodium is the key to finding the cause — and the cause drives the treatment.
Low serum osmolality (hypotonic)
This is the most common type. Sort it further by the patient's fluid (volume) status:
Hypovolemic (low fluid)
Low volume and low osmolality. Causes: dehydration, diuretics, Addison's disease (if dehydrated), and third-spacing (severe burns or pancreatitis).
Euvolemic (normal fluid)
Normal volume, low osmolality. Causes: SIADH, severe hypothyroidism, adrenal insufficiency, some antidepressants/antipsychotics, and psychogenic polydipsia.
Hypervolemic (high fluid)
Fluid overload with low osmolality. Causes: heart failure (CHF), end-stage renal disease, cirrhosis, and nephrotic syndrome.
What is SIADH? The body makes too much ADH, so it retains excess water and dilutes the blood's sodium. It's classically euvolemic. Triggers include lung or brain cancers, pneumonia/tuberculosis, brain disorders (meningitis, stroke), and certain medications (some antidepressants and chemo drugs).
Normal serum osmolality (isotonic)
Relatively rare. Lab artifact from substances crowding the plasma:
Hyperproteinemia
Very high protein (e.g., multiple myeloma) displaces plasma water, lowering measured sodium — "pseudohyponatremia."
Severe Hyperlipidemia
Very high lipids (e.g., severe hypertriglyceridemia) cause the same lab artifact and a falsely low sodium.
High serum osmolality (hypertonic)
Driven by other osmotically active substances pulling water into the bloodstream:
Hyperglycemia
High blood sugar draws water out of cells, diluting sodium. Osmotic diuresis then causes dehydration, so osmolality can end up normal or low.
Mannitol
A sugar-alcohol diuretic (used for raised ICP) that increases serum osmolality and can cause hypertonic hyponatremia.
Causes of hyponatremia organized by serum osmolality and volume status.
Nursing Assessment of Hyponatremia
Symptoms vary with severity and especially with how fast the sodium dropped. Many are neurologic, driven by brain-cell swelling.
Common symptoms
Fatigue
Low sodium interferes with energy production, causing tiredness and lethargy.
Headache
Often one of the earliest symptoms.
Nausea & Vomiting
Common — and vomiting can worsen hyponatremia by losing more sodium and water.
Weakness & Cramps
Sodium is needed for muscle contraction; low levels cause weakness, cramps, or spasms.
Altered Mental Status
Confusion, disorientation, poor concentration — and in severe cases, loss of consciousness or coma from brain swelling.
Seizures
In severe hyponatremia, rapid brain-cell swelling can trigger seizures.
Don't Forget Fall Risk
Weakness, fatigue, and altered mental status make these patients a fall risk. Put the bed alarm on and make sure they're in fall-risk socks.
Physical assessment
Vital Signs
BP may be low with dehydration or high with heart failure/kidney disease; heart rate may rise to compensate for low BP.
Neuro Assessment
Check mental status, gait, and coordination. Severe cases cause cerebral edema and raised ICP — watch for dilated/sluggish or asymmetric pupils.
Cardiac Assessment
May reveal heart failure clues — an S3, dependent edema, or JVD. Note: sodium abnormalities do not typically cause significant arrhythmias.
Skin Assessment
Dry skin/mucous membranes, sunken eyes, or poor skin turgor suggest dehydration — a common cause of hypotonic hyponatremia.
Treatment is really about treating the underlying cause. In severe cases, nephrology is typically consulted. The main components:
Address the Underlying Causethe actual treatment
Identify and manage whatever is driving the low sodium. This usually means adjusting fluids — increasing or decreasing them depending on volume status.
IV Fluidsfor fluid deficit
IV fluids like sodium chloride carry sodium and are used when there's a fluid deficit — correcting the deficit usually corrects the sodium. Cautious boluses may be followed by maintenance fluids until hydration and sodium normalize.
Fluid Restrictionfor water excess / overload
When hyponatremia is from excess water intake, retention, or fluid overload, restricting fluids is often first-line and gradually raises serum sodium.
Sodium Replacementoral tablets or hypertonic saline
Oral sodium tablets help patients with low dietary intake, potomania, or sodium-wasting meds (like Lasix); SIADH may be treated with sodium tablets plus Lasix and fluid restriction. In acute or severe cases, IV 3% hypertonic saline is used — typically 100 mL bolus over 10 min.
Medicationfor SIADH
SIADH may be treated with vasopressin receptor antagonists (which block ADH). Urea can also be used to increase loss of electrolyte-free water.
The general goal is to raise sodium by 4–6 mEq/L in the first 24 hours for most cases (within ~6 hours in severe, symptomatic cases). Acute hyponatremia can be corrected somewhat more aggressively; chronic hyponatremia must be corrected especially slowly.
Correct Too Fast = ODS
Raising sodium too quickly can cause osmotic demyelination syndrome (ODS), an irreversible destruction of the myelin sheath around nerve fibers. To prevent it, sodium should never be corrected more than 8 mEq/L in 24 hours in chronic hyponatremia.
Monitoring of Hyponatremia
Monitor closely to catch both under- and over-correction:
Lab Tests
Check sodium frequently — every 2–4 hours in severe cases, at least every 24 hours otherwise — plus other electrolytes and renal function.
Neuro Status
Reassess consciousness, orientation, strength, and coordination. Report new confusion, seizures, or loss of consciousness immediately.
Intake & Output
Document I&Os thoroughly to track the patient's fluid balance.
Clinical Pearls
1
Always pair sodium with osmolality and volume status. That combination is what reveals the cause — and the cause drives the treatment.
2
Correct chronic hyponatremia slowly. No more than 8 mEq/L in 24 hours to avoid irreversible ODS.
3
SIADH is the classic euvolemic cause. Too much ADH, water retention, dilutional low sodium — think lung/brain pathology and meds.
4
Sodium rarely causes arrhythmias. Unlike potassium or calcium, the danger here is neurologic — brain-cell swelling, not the ECG.
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